TRIM31: A Novel Guardian Against Periodontal Inflammation via Modulation of NLRP3 Inflammasome and Macrophage Polarization.

IF 2.3 4区 医学 Q3 IMMUNOLOGY
Immunological Investigations Pub Date : 2026-10-01 Epub Date: 2026-06-22 DOI:10.1080/08820139.2026.2680504
Xiaolu Zhang, Dazhuang Lu, Lijia Lin, Weijuan Qi, Shan He
{"title":"TRIM31: A Novel Guardian Against Periodontal Inflammation via Modulation of NLRP3 Inflammasome and Macrophage Polarization.","authors":"Xiaolu Zhang, Dazhuang Lu, Lijia Lin, Weijuan Qi, Shan He","doi":"10.1080/08820139.2026.2680504","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Periodontitis involves dysregulated immunity where the NLRP3 inflammasome plays a key role, while the role of TRIM31, an E3 ubiquitin ligase, remains unknown in periodontitis.</p><p><strong>Methods: </strong>Human gingival fibroblasts (HGFs) and macrophages were stimulated with LPS and ATP; TRIM31 was overexpressed via AAV, and NLRP3 was knocked out via CRISPR; periodontitis was induced in WT and NLRP3-KO mice treated with AAV-TRIM31; bone loss, osteoclasts, and apoptosis were assessed.</p><p><strong>Results: </strong>TRIM31 was downregulated in inflammation and correlated with M2 polarization. TRIM31 overexpression protected HGFs, promoted M2 polarization, and bound to NLRP3, thereby promoting K48-linked ubiquitination and degradation. In vivo, TRIM31 reduced bone loss, osteoclasts, and apoptosis; these effects were abolished in NLRP3-KO cells and mice.</p><p><strong>Conclusion: </strong>TRIM31 negatively regulates periodontal inflammation via ubiquitin-dependent NLRP3 degradation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1372-1392"},"PeriodicalIF":2.3000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunological Investigations","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/08820139.2026.2680504","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/6/22 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Periodontitis involves dysregulated immunity where the NLRP3 inflammasome plays a key role, while the role of TRIM31, an E3 ubiquitin ligase, remains unknown in periodontitis.

Methods: Human gingival fibroblasts (HGFs) and macrophages were stimulated with LPS and ATP; TRIM31 was overexpressed via AAV, and NLRP3 was knocked out via CRISPR; periodontitis was induced in WT and NLRP3-KO mice treated with AAV-TRIM31; bone loss, osteoclasts, and apoptosis were assessed.

Results: TRIM31 was downregulated in inflammation and correlated with M2 polarization. TRIM31 overexpression protected HGFs, promoted M2 polarization, and bound to NLRP3, thereby promoting K48-linked ubiquitination and degradation. In vivo, TRIM31 reduced bone loss, osteoclasts, and apoptosis; these effects were abolished in NLRP3-KO cells and mice.

Conclusion: TRIM31 negatively regulates periodontal inflammation via ubiquitin-dependent NLRP3 degradation.

TRIM31:通过调节NLRP3炎性体和巨噬细胞极化来对抗牙周炎症的新守护者。
背景:牙周炎涉及免疫失调,其中NLRP3炎性体起关键作用,而TRIM31 (E3泛素连接酶)在牙周炎中的作用尚不清楚。方法:LPS和ATP刺激人牙龈成纤维细胞(HGFs)和巨噬细胞;TRIM31通过AAV过表达,NLRP3通过CRISPR敲除;AAV-TRIM31诱导WT和NLRP3-KO小鼠牙周炎;评估骨丢失、破骨细胞和细胞凋亡。结果:TRIM31在炎症中下调,与M2极化相关。TRIM31过表达可保护hgf,促进M2极化,并与NLRP3结合,从而促进k48相关的泛素化和降解。在体内,TRIM31可减少骨质流失、破骨细胞和细胞凋亡;这些作用在NLRP3-KO细胞和小鼠中被消除。结论:TRIM31通过降解泛素依赖性NLRP3负向调节牙周炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Immunological Investigations
Immunological Investigations 医学-免疫学
CiteScore
5.50
自引率
7.10%
发文量
49
审稿时长
3 months
期刊介绍: Disseminating immunological developments on a worldwide basis, Immunological Investigations encompasses all facets of fundamental and applied immunology, including immunohematology and the study of allergies. This journal provides information presented in the form of original research articles and book reviews, giving a truly in-depth examination of the latest advances in molecular and cellular immunology.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书